Ventilatory responses to hypercapnia and hypoxia during continuous aspirin ingestion

Hypercapnic and hypoxic ventilatory responses were serially measured in nine normal subjects given 3.9 g aspirin (ASA) per day for 9 days. Minute ventilation (V̇E), end-tidal carbon dioxide tension (PET(CO₂)), venous bicarbonate concentration [HCO₃^-], oxygen consumption (V̇O₂), consumption (VO₂), hypercapnic ventilatory response (ΔV̇E/ΔPCO₂), and isocapnic hypoxic ventilatory response (A) were determined before, 2 h after the first dose, and at 72-h intervals during the next 14 days. Serum salicylate levels averaged 18.6 ± 2.0 mg/dl. V̇E increased (P<0.05), PET(CO₂) decreased (P <0.05), and [HCO₃^-] did not change significantly during drug ingestion. ΔV̇E/ΔPCO₂ increased gradually to a value 37% greater than control by day 3 and reamined constant (P <0.01). A increased by 251% and VO₂ by 18% within 2 h and remained constant for the reaminder of the ASA period (P <0.01). All values returned to base line within 24 h following cessation of ASA. We concluded that during continuous ASA ingestion there is a gradual increase of hypercapnic ventilatory response. This may reflect slow entrance of ASA into the central nervous system. In contrast, there is a rapid rise in hypoxic ventilatory response which may be mechanistically linked to changes in metabolic rate.